Cocoa powder, derived from Theobroma cacao, is a popular food ingredient that is commonly consumed in chocolate. The ingredient is rich in fiber, iron and phytochemicals which provide positive health benefits such as antioxidant polyphenols and methylxanthines.
Epidemiological and human intervention studies have reported that chocolate is associated with reduced risk of cardiometabolic diseases and lab studies suggest dietary supplementation with cocoa or cocoa polyphenols can improve obesity and obesity-related comorbidities, including non-alcoholic fatty liver disease (NAFLD).
Limited studies have examined the effect of cocoa/chocolate on NAFLD and underlying hepatoprotective mechanisms, which is why researchers from Penn State University took on the challenge of examining the hepatoprotective effects of cocoa dietary supplementation.
"While it is typically considered an indulgence food because of its high sugar and fat content, epidemiological and human-intervention studies have suggested that chocolate consumption is associated with reduced risk of cardio-metabolic diseases including stroke, coronary heart disease and Type 2 diabetes," explained study leader Joshua Lambert, professor of food science in the College of Agricultural Sciences. "So, it made sense to investigate whether cocoa consumption had an effect on non-alcohol-related fatty liver disease, which is commonly associated with human obesity."
Study design
Using a high-fat-fed, diet-induced model of obesity, the research team supplemented mice with 80 mg cocoa powder per gram of food for 10 weeks. The cocoa was a commercially available product at a "physiologically achievable dose" —making it possible to duplicate the dosage in humans.
“For people it works out to about 10 tablespoons of cocoa powder a day," Lambert said. "Or, if you follow the directions on the Hershey's box of cocoa powder, that's about five cups of hot cocoa a day."
According to Lambert, this high-fat-fed, diet-induced obesity model simulates the current public health situation related to NAFLD. Lambert noted that because so many people a large portion have preexisting obesity and NAFLD, there is a need to develop potentially effective dietary interventions rather than just preventive agents.
The research team examined changes in fatty liver disease, markers of oxidative stress, antioxidant response and cell damage in high-fat-fed obese mice treated with a diet.
Findings
The researchers found that cocoa-treated mice gained weight at a 22% lower rate and had smaller spleen weights than the high-fat-fed control mice. The smaller spleen weights are indicative of less inflammation.
At the end of the study, mice fed the cocoa-powder-supplemented diet had 28% less fat in their livers than the control mice. Cocoa-treated mice also had 57% lower levels of oxidative stress and 75% lower levels of DNA damage in the liver compared to high-fat-fed control mice.
According to the report, these changes were associated with higher hepatic superoxide dismutase and glutathione peroxidase enzyme activity and increased expression of hepatic mitochondrial biogenesis markers.
“Our results indicate that cocoa supplementation can mitigate the severity of NAFLD in obese mice and that these effects are related to sirtuin 3/peroxisome proliferator activated receptor g coactivator1a-mediated increases in antioxidant response and mitochondrial biogenesis,” the authors noted.
Mechanisms of action
Previous studies in Lambert’s lab suggest that extracts from cocoa and some of the chemicals in cocoa powder can inhibit the enzymes that are responsible for digesting dietary fat and carbohydrates.
Lambert suggested that when mice get cocoa as part of their diet, these compounds in the cocoa powder prevent dietary fat digestion. When fat can't be absorbed, it passes through the digestive system. To the delight of many, Lambert believes a similar process could happen with humans.
Source: Journal of Nutritional Biochemistry
https://doi.org/10.1016/j.jnutbio.2021.108618
“Dietary cocoa ameliorates non-alcoholic fatty liver disease and increases markers of antioxidant response and mitochondrial biogenesis in high fat-fed mice”
Authors: M. Sun et al.